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Multifunctional transcription factor in ER stress response. Plays an essential role in the response to a wide variety of cell stresses and induces cell cycle arrest and apoptosis in response to ER stress. Plays a dual role both as an inhibitor of CCAAT/enhancer-binding protein (C/EBP) function and as an activator of other genes. Acts as a dominant-negative regulator of C/EBP-induced transcription: dimerizes with members of the C/EBP family, impairs their association with C/EBP binding sites in the promoter regions, and inhibits the expression of C/EBP regulated genes. Positively regulates the transcription of TRIB3, IL6, IL8, IL23, TNFRSF10B/DR5, PPP1R15A/GADD34, BBC3/PUMA, BCL2L11/BIM and ERO1L. Negatively regulates; expression of BCL2 and MYOD1, ATF4-dependent transcriptional activation of asparagine synthetase (ASNS), CEBPA-dependent transcriptional activation of hepcidin (HAMP) and CEBPB-mediated expression of peroxisome proliferator-activated receptor gamma (PPARG). Inhibits the canonical Wnt signaling pathway by binding to TCF7L2/TCF4, impairing its DNA-binding properties and repressing its transcriptional activity. Plays a regulatory role in the inflammatory response through the induction of caspase-11 (CASP4/CASP11) which induces the activation of caspase-1 (CASP1) and both these caspases increase the activation of pro-IL1B to mature IL1B which is involved in the inflammatory response.

This gene encodes a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors. The protein functions as a dominant-negative inhibitor by forming heterodimers with other C/EBP members, such as C/EBP and LAP (liver activator protein), and preventing their DNA binding activity. The protein is implicated in adipogenesis and erythropoiesis, is activated by endoplasmic reticulum stress, and promotes apoptosis. Fusion of this gene and FUS on chromosome 16 or EWSR1 on chromosome 22 induced by translocation generates chimeric proteins in myxoid liposarcomas or Ewing sarcoma. Multiple alternatively spliced transcript variants encoding two isoforms with different length have been identified. [provided by RefSeq, Aug 2010]

CGK733-induced intracellular calcium sequestration in pancreatic tumor cells is correlated with the PERK/CHOP signaling pathway and may also be involved in the dysregulations of calcium-binding proteins.

Combined administration inhibited the cells most potently and time-dependently, decreased the expression of HO-1, and significantly increased the expression of ATF4, CHOP, and Ire-1 proteins expression levels

These data show that altered/impaired expression of mtDNA induces CHOP-10 expression in a signaling pathway that depends on the eIF2alpha/ATF4 axis of the integrated stress response rather than on the mitochondrial unfolded protein response.

this study for the first time provided substantial evidence for the FUS-CHOP oncoprotein as an inducer of metastasis that is due to the transcriptional induction of specific tumor-associated proteases.

Findings demonstrate that CypB prevents hypoxia-induced cell death through modulation of ubiquitin-mediated CHOP protein degradation, suggesting that CypB may have an important role in the tight regulation of CHOP under hypoxia.

azadirone can sensitize cancer cells to TRAIL through ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins, and up-regulation of proapoptotic proteins.

These results suggested a potential regulatory function of L-cysteine which may lead to changes in global conformation of CHOP in response to the cellular redox state and/or endoplasmic reticulum stress.

DDIT3, STT3A, ARG2 and FAM129A immunohistochemistry does not appear to be useful in the diagnosis of thyroid follicular neoplasias, as they do not reliably distinguish follicular thyroid carcinoma from follicular thyroid adenoma.

The formation of the spliced variant of XBP1s was detectable in 16.2% of AML patients, and consistent with activated unfolded protein response, thess patients also had significantly increased expression of calreticulin, GRP78, and CHOP.

Up regulation of GADD-153, GRP-78, with more pronounced expression in proliferative glomerulonephritis(GN) vs. nonproliferative GN and down regulation of Bcl-2 proteins was observed in the GN as compared to minimal change disease

The FUS-DDIT3 protein induces increased expression of the CAAT/enhancer-binding protein (C/EBP) and nuclear factor-kappaB (NF-kappaB)-controlled gene IL8, and the N-terminal FUS part is required for this activation.

These results suggest that Stx2-induced apoptosis is mediated by CHOP in human brain microvascular endothelial cells (HBMEC) and involves activation of both the intrinsic and extrinsic pathways of apoptosis.

results suggest that the presence of MELAS and NARP mtDNA mutations elicits upregulation of CHOP and ASNS genes through the elevation of ATF4 expression and its binding to the amino acid regulatory element and nutrient-sensing response element-1

Expression of Rad51 enhances basal- and HIV-1 Tat-induced transcription of the HIV-1 LTR promoter; this event requires cooperativity from the C/EBP family of transcription factors including C/EBPbeta and C/EBPbeta homologous protein (CHOP)

CRP induced an increase of GADD153 mRNA expression. CRP regulation of GADD153 in VSMCs occurs at the posttranscriptional level by mRNA stabilization. GADD153 colocalized to apoptotic VSMCs in coronary lesions, supporting a role in CRP-induced cell death.

These results suggest that GADD153 overexpression induced by N-(4-hydroxyphenyl)retinamide(4HPR) may contribute to the anticancer effects (induction of apoptosis and growth arrest) of 4HPR on cancer cells.

Azadirone, a limonoid tetranortriterpene, induces death receptors and sensitizes human cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) through a p53 protein-independent mechanism: evidence for the role of the ROS-ERK-CHOP-death receptor pathway.

Interleukin-8 overexpression in astrocytomas is induced by prostaglandin E2 and is associated with the transcription factors CCAAT/enhancer-binding protein-? and CCAAT/enhancer-binding homologous protein.